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Caloric restriction (CR) is a widely recognized geroprotective intervention that slows or prevents Alzheimer's disease (AD) in animal models. CR is typically implemented via feeding mice a single meal per day; as CR mice rapidly consume their food, they are subject to a prolonged fast between meals. While CR has been shown to improve metabolic and cognitive functions and suppress pathological markers in AD mouse models, the specific contributions of fasting versus calorie reduction remains unclear. Here, we investigated the contribution of fasting and energy restriction to the beneficial effects of CR on AD progression. To test this, we placed 6-month-old 3xTg mice on one of several diet regimens, allowing us to dissect the effects of calories and fasting on metabolism, AD pathology, and cognition. We find that energy restriction alone, without fasting, was sufficient to improve glucose tolerance and reduce adiposity in both sexes, and to reduce Aβ plaques and improve aspects of cognitive performance in females. However, we find that a prolonged fast between meals is necessary for many of the benefits of CR, including improved insulin sensitivity, reduced phosphorylation of tau, decreased neuroinflammation, inhibition of mTORC1 signaling, and activation of autophagy, as well as for the full cognitive benefits of CR. Finally, we find that fasting is essential for the benefits of CR on survival in male 3xTg mice. Overall, our results demonstrate that fasting is required for the full benefits of a CR diet on the development and progression of AD in 3xTg mice, and suggest that both when and how much we eat influences the development and progress of AD.
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http://dx.doi.org/10.1101/2024.09.19.613904 | DOI Listing |
J Prev Alzheimers Dis
September 2025
Omphalos Bioscience LLC, Sandia Park NM 87047, USA.
Four studies now document reduced incidence of Alzheimer's disease (AD) or dementia diagnoses in aging individuals who report higher dietary intake of flavonols (or their glycosides) years prior to diagnosis vs those with lower intake. These effects are large, almost 50 %, for individuals at higher genetic risk for AD, providing a robust gene x environment interaction. They display a specific structure-activity relationship.
View Article and Find Full Text PDFNeuromolecular Med
September 2025
Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México (UNAM), Cuidad Universitaria, Apartado Postal 70228, CP 04510, CDMX, Mexico.
It is now widely accepted that the development of neurodegenerative diseases depends on and affects many pathological processes, both in the brain and the periphery. Inflammatory, cardiovascular, metabolic, cerebrovascular, autoimmune, and other environmental factors have been extensively studied and shown to contribute notably to the onset, pathogenesis, and clinical outcome of Alzheimer´s disease (AD), Parkinson´s disease (PD), cerebral amyloid angiopathy (CAA), multiple sclerosis, and other neurological disorders. Likewise, AD-induced changes in other tissues outside the central nervous system, such as abnormalities observed in the liver, spleen, or lungs, have been documented and extensively studied, leading to a better understanding of brain-periphery crosstalk in neurodegenerative diseases and the development of novel diagnostic and therapeutic approaches.
View Article and Find Full Text PDFArtery structural properties and Alzheimer's disease (AD) pathology are individually associated with impaired cerebrovascular function; however, the interaction of these factors is unclear. Furthermore, while elastin haploinsufficient (Eln+/-) mice are known to have impaired cerebrovascular function, sex differences for this effect have not been previously studied. To answer these questions, we crossed middle-aged and old Eln+/-mice with 3xTg-AD mice.
View Article and Find Full Text PDFMetab Brain Dis
August 2025
Laboratory Animal Centre, Model Animal and Human Disease Research of Luzhou Key Laboratory, Southwest Medical University, Luzhou, China.
As a neurodegenerative disease characterized by progressive cognitive decline, the pathogenesis of Alzheimer's disease (AD) is still poorly understood, and there is no effective cure currently available. Traditional Chinese medicine (TCM) prescription Yangming-Kaixin-Yizhi formula (YKY) has been clinically applied for the treatment of memory loss related disorders for more than 300 years with remarkable efficacy, but its pharmacological mechanism remains unclear. This study aimed to investigate the therapeutic effects of YKY on AD and its molecular mechanisms.
View Article and Find Full Text PDFNeurotherapeutics
August 2025
Faculty of Life and Health Sciences, Shenzhen University of Advanced Technology (SUAT), Shenzhen, Guangdong 518055, China. Electronic address:
Asparagine endopeptidase (AEP) plays a critical role in Alzheimer's disease (AD) by cleaving amyloid precursor protein (APP) at N585 and tau protein at N368. Genetic deletion or pharmacological inhibition of AEP using compound 11a ameliorates AD pathology in murine models. To improve the therapeutic potential of 11a, we synthesized structural analogs and developed a zein-based nanoparticle delivery system to enhance pharmacokinetics.
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